Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of a single administration of hepatotoxic chemicals on the major gap-junction protein of liver (connexin 32) were studied in rats. The connexin-32 content was analyzed by immunoblotting and immunohistochemistry using an affinity-purified monoclonal antibody against connexin 32. The connexin-32 content decreased dramatically to less than 10% of the control value 24 h after injection of 25 mg/kg dimethylnitrosamine and returned to the normal level 240 h later. Injection of CCl4 at a dose of 1 ml/kg also caused a transient reduction of connexin-32 content in the liver, as seen after the dimethylnitrosamine injection. The decrease in hepatic connexin-32 content was inversely correlated to the increase in plasmic alanine-aminotransferase activity which has been used as an index of acute liver injury. The changes in connexin 32 were essentially similar to those observed in regenerating liver after partial hepatectomy. However, incorporation of [3H]thymidine into liver DNA after dimethylnitrosamine injection was significantly less than that obtained after partial hepatectomy. The 5'-nucleotidase activity of the plasma-membrane fraction of the liver was not significantly altered by the injection of dimethylnitrosamine. These results suggest that liver gap-junction protein is specifically reduced by acute liver injury and that this kind of decrease in connexin 32 is not simply related to cell proliferation, unlike the decrease after partial hepatectomy.
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PMID:Single administration of hepatotoxic chemicals transiently decreases the gap-junction-protein levels of connexin 32 in rat liver. 184 85

The ability of 14 serum biochemical assays to predict the presence of hepatic necrosis induced by carbon tetrachloride (CCl4) (centrilobular necrosis), allyl alcohol (periportal necrosis), and 1-napththylisothiocyanate (ANIT) (biliary duct necrosis) was evaluated in rats. Results of these assays were analyzed using multivariate discriminant analysis to determine: which assays have the highest predictive value for discriminating between control and treated rats, and which assays would discriminate between rats in the three treatment groups. Individual assays with the highest predictive value for CCl4-induced lesions versus controls were glutamate dehydrogenase (GDH), sorbitol dehydrogenase (SDH), and alanine aminotransferase (ALT). Assays with the highest predictive value for ANIT-induced lesions were GDH, 5'-nucleotidase (5'NT), and ALT. Assays the highest predictive value for ANIT-induced lesions were GDH, 5'-nucleotidase (5'NT), and ALT. Assays with the highest predictive value for allyl alcohol-induced lesions were an ALT/isocitrate dehydrogenase (ICD) ratio, GDH, and ALT. Canonical correlation coefficients for each assay ranged from 0.98 to 0.91 with 95-100% correct group membership predictions (treated versus control) provided by each assay. Individual assays were not highly predictive for determining group membership among all three treatment groups. A two assay combination of 5'NT and an ALT/ICD ratio provided 100% correct group membership predictions and had high canonical correlations (f1 = 0.95, f2 = 0.83).
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PMID:Evaluating toxin-induced hepatic injury in rats by laboratory results and discriminant analysis. 301 5

5'-Nucleotidase activity an enzyme marker of the plasma membranes, increases in female rat liver homogenates following ethionine administration, while homogenates from males show no changes. Treatment with CCl4, colchicine, cycloheximide, emetine, ethanol and 5-fluorotryptophan does not significantly modify the 5'-nucleotidase activity of liver homogenates of either female or male rats.
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PMID:5'-Nucleotidase activity in liver homogenates of rats treated with CCl4, colchicine, cycloheximide, emetine, ethanol, ethionine and 5-fluorotryptophan. 625 41

The effect of carrot extract on carbon tetrachloride (CCl4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl4 administration. Increased activities of hepatic 5'-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl4-induced hepatocellular injury.
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PMID:Hepatoprotective activity of carrot (Daucus carota L.) against carbon tetrachloride intoxication in mouse liver. 750 Jun 38

The chemoprotection extended by eugenol against carbon tetrachloride (CCl4) intoxication was established by studies on drug-metabolizing phase I and phase II enzymes. An overall decrease in drug-metabolizing enzymes, namely NADPH-cytochrome c reductase, NADH-cytochrome reductase, coumarin hydroxylase, 7-ethoxy coumarin-O-deethylase, UDP-glucuronyltransferase and glutathione-S-transferase, was observed with CCl4 intoxication, with a subsequent decrease in cytochrome P450 and cytochrome b5 content. CCl4 caused a significant decrease in microsomal phospholipids and the marker enzymes glucose-6-phosphatase and 5'-nucleotidase, and an increase in thiobarbituric acid reactive substances (TBARS). Simultaneous administration of eugenol with CCl4 inhibited the accumulation of TBARS and the decrease in the microsomal phospholipids and marker enzymes. Further, the chemical onslaught imposed by CCl4 on the drug-metabolizing system was removed successfully by eugenol. Eugenol appears to act as an in vivo antioxidant and as a better inducer of phase II enzymes than phase I enzymes. It is therefore suggested that eugenol could be an interesting basic structure for drug design.
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PMID:Effect of eugenol on drug-metabolizing enzymes of carbon tetrachloride-intoxicated rat liver. 778 11

Because groundwater contamination is an important environmental concern, we examined the hepatic and renal effects of repeated exposure to a mixture of 25 chemicals frequently found in groundwater near hazardous-waste disposal sites and the effect of such exposure on carbon tetrachloride (CCI4) toxicity. Adult male F-344 rats received ad libitum deionized water and feed (Ad Lib Water) or ad libitum 10% MIX (referring to 10% of a technically achievable stock mixture) and feed for 14 d. Because exposure to the 25-chemical mixture via the drinking water resulted in decreased water and feed consumption, restricted deionized water and feed controls (Restricted Water) were included. On d 14, rats were gavaged with 0, 0.0375, 0.05, 0.075 or 0.15 ml CCl4/kg, and hepatic and renal toxicity assessed 24 h later. Little or no hepatic and renal toxicity was observed in rats exposed to 10% MIX alone. No hepatic or renal lesions occurred that could be attributed to 10% MIX alone. Slight but statistically significant alterations, of uncertain biological significance, resulted from the water treatments: 10% MIX increased alanine aminotransferase, urea nitrogen (BUN), and BUN/creatinine ratio; Restricted Water increased 5'-nucleotidase and decreased alkaline phosphatase. Relative kidney weight was increased by both 10% MIX and Restricted Water. CCI4 resulted in significant dosage-dependent hepatotoxicity in all three water treatment groups but had little or no effect on renal indicators of toxicity. Relative to Ad Lib Water, significantly greater hepatotoxicity occurred in both 10% MIX and Restricted Water rats. The response to CCI4 in the Restricted Water rats was similar to that of 10% MIX rats, indicating that a substantial portion of the effect of 10% MIX on CCI4 hepatotoxicity is due to decreased water and feed intake.
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PMID:Toxicology studies of a chemical mixture of 25 groundwater contaminants: hepatic and renal assessment, response to carbon tetrachloride challenge, and influence of treatment-induced water restriction. 796 40

Previous results in male Sprague-Dawley rats indicate that acetone (A), methyl ethyl ketone (MEK), and methyl isobutyl ketone (MiBK) pretreatments (3 d, p.o.) at a dosage of 6.8 mmol/kg potentiate CCl4 hepatotoxicity. The potentiation potency profile observed was MiBK > A > MEK. In the present study, male Sprague-Dawley rats were treated for 3 d with 6.8 mmol/kg (p.o.) of A, MEK, or MiBK using Emulphor as vehicle (10 ml/kg). Rats were either killed 18 h after the last pretreatment or treated with CCl4 (prepared in corn oil) and then killed 48 h later. Livers were perfused; purified plasma membrane (PM), sinusoidal (SM) and basal canalicular membrane (BCM) fractions were prepared. Membrane fluidity was monitored by fluorescence polarization using 1,6-diphenyl-1,3,5-hexatriene (DPH) or 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). The following membrane enzymes were measured to monitor membrane purity and treatment effects: 5'-nucleotidase (5N), leucine aminopeptidase (LAP), and alkaline phosphatase (AP). Our results suggest that CCl4 modifies membrane integrity as indicated by a decrease in liver membrane 5N, LAP, and AP activity. CCl4 also increased the fluidity of the lipid and protein portions of the liver membranes as measured by the DPH and TMA-DPH fluorescence probes, respectively. Of the three ketones, only A altered CCl4 effects on plasma membrane enzymes and decreased BCM fluidity. The data only partially support increased susceptibility of liver membranes by ketone pretreatment as a factor implicated in the mechanism of potentiation of CCl4-induced hepatotoxicity.
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PMID:Ketone potentiation of haloalkane-induced hepatotoxicity: CCl4 and ketone treatment on hepatic membrane integrity. 887 55